2012 年 8 巻 2 号 p. 168-173
Regular exercise plays an important role in preventing metabolic diseases, the impairment of cognitive function, and the onset of depression. Regular exercise enhances adult neurogenesis in the dentate gyrus of the hippocampus, and the exercise-derived prevention of cognitive deficits and depression is closely related to adult hippocampal neurogenesis. Both blood-derived factors and brain-derived factors are thought to contribute to the exercise-induced enhancement of adult hippocampal neurogenesis. Blood-derived factors include insulin-like growth factor 1 (IGF-1) and vascular endothelial growth factor (VEGF) . Exercise increases the transport of these substances from the blood to the brain and increases adult hippocampal neurogenesis. In contrast the exercise-induced enhancement of adult hippocampal neurogenesis can be blocked by inhibiting the binding of IGF-1 or VEGF to its receptor. On the other hand, brain-derived factors include brain-derived neurotrophic factor (BDNF) or Wnt3. In particular, BDNF plays a wide range of roles in neuronal development and survival, and the exercise-induced enhancement of hippocampal BDNF contributes to the increase in hippocampal neurogenesis. Aging and chronic stress impairs cognitive function, whereas regular exercise prevents age- or stress-induced impairment of cognitive function, the improvement of which is attributed to the action of IGF-1 or BDNF. In addition, the preventive effect of exercise on the onset of depression is also dependent on the improvement of hippocampal neurogenesis via BDNF or VEGF. These findings demonstrate that regular exercise helps maintain cognitive function and prevents depression in the elderly and the stressed; however, the mechanism of the exercise-induced improvement of cognition or depression remains unclear. Clarifying the mechanism via neuroscientific and molecular biological studies is needed to promote the usefulness of exercise for preventing cognitive deficits and depression.